MicroRNA 24-3p (miR-24-3p)

MicroRNA 24-3p (miR-24-3p) is a mature, highly conserved non-coding RNA molecule approximately 22 nucleotides in length that plays a central role in the post-transcriptional regulation of gene expression [1, 5, 12]. It functions by binding to the 3'-untranslated regions (3'-UTRs) of a diverse array of messenger RNAs, such as Notch1, Bcl-2L11 (BIM), and ATG4A, leading to their degradation or the inhibition of their translation [1, 3, 6, 9]. This molecule is an essential regulator of fundamental cellular processes, including cell cycle progression, apoptosis, and angiogenesis [4, 10, 15]. In clinical settings, miR-24-3p is frequently dysregulated and can act as either an oncomiR or a tumor suppressor depending on the tissue environment, and its altered levels are notably implicated in cardiovascular diseases, neurodegeneration (such as Multiple Sclerosis), and chronic respiratory conditions like COPD [2, 7, 11, 12]. Although no miR-24-3p-specific drugs have yet reached the market, it is a significant therapeutic target being explored via antisense antagomirs to inhibit its pathological overexpression or miRNA mimics to restore its protective functions in various disease states [5, 18, 19].

Other names

hsa-miR-24-3phsa-miR-24miRNA-24miR-24MicroRNA 24MIR24

miR-24-3p acts through RNA interference (RNAi), where it guides the RNA-induced silencing complex (RISC) to bind complementary sequences in target mRNAs, resulting in translational repression or mRNA degradation. Therapeutic modulation typically involves antisense oligonucleotides (antagomirs) that sequester the mature miRNA to prevent it from binding its targets or miRNA mimics that introduce exogenous miR-24-3p to restore its regulatory activity.